# Long-term interleukin-1α treatment inhibits insulin signaling via IL-6 production and SOCS3 expression in 3T3-L1 adipocytes
> Uno T.

URL kanonis: https://discover.unhas.ac.id/publications/long-term-interleukin-1-treatment-inhibits-insulin-signaling-via-il-6-production
Jurnal / Konferensi: Hormone and Metabolic Research
Tahun terbit: 2008
DOI: https://doi.org/10.1055/s-2007-1004515
ISSN: 00185043
Kuartil SJR: Q2
Citations: 20

## Authors
- Uno T.

## Abstract
Proinflammatory cytokines are well-known to inhibit insulin signaling to result in insulin resistance. IL-1alpha is also one of the proinflammatory cytokines, but the mechanism of how IL-1alpha induces insulin resistance remains unclear. We have now examined the effects of IL-1alpha on insulin signaling in 3T3-L1 adipocytes. Prolonged IL-1alpha treatment for 12 to 24 hours partially decreased the protein levels as well as the insulin-stimulated tyrosine phosphorylation of IRS-1 and Akt phosphorylation. mRNA for SOCS3, an endogenous inhibitor of insulin signaling, was dramatically augmented 4 hours after IL-1alpha treatment. Concomitantly, the level of IL-6 in the medium and STAT3 phosphorylation were increased by the prolonged IL-1alpha treatment. Addition of anti-IL-6 neutralizing antibody to the medium or overexpression of dominant-negative STAT3 decreased the IL-1alpha-stimulated STAT3 activation and SOCS3 induction, and ameliorated insulin signaling. These results suggest that the IL-1alpha-mediated deterioration of insulin signaling is largely due to the IL-6 production and SOCS3 induction in 3T3-L1 adipocytes.

## Keywords
- SOCS3
- Proinflammatory cytokine
- Tyrosine phosphorylation
- Endocrinology
- Internal medicine
- Insulin
- Insulin resistance
- Phosphorylation
- 3T3-L1
- Insulin receptor
- Protein kinase B
- Signal transduction
- Chemistry
- Cytokine
- STAT3
- Insulin receptor substrate
- Biology
- Medicine
- Cell biology
- Inflammation
- Adipose tissue
- Adipocyte

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Sumber: Discover Unhas — RIMS Universitas Hasanuddin.
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